DOI QR코드

DOI QR Code

A biodegradable magnesium alloy sample induced rat osteochondral defect repair through Wnt/β-catenin signaling pathway

  • Zhao, Kexin (Department of Bone & Joint Surgery, Peking University Shenzhen Hospital, Shenzhen Peking UniversityThe Hong Kong University of Science and Technology Medical Center) ;
  • Chen, Yingqi (Department of Bone & Joint Surgery, Peking University Shenzhen Hospital) ;
  • Yu, Fei (Department of Bone & Joint Surgery, Peking University Shenzhen Hospital) ;
  • Jian, Weng (Department of Bone & Joint Surgery, Peking University Shenzhen Hospital) ;
  • Zheng, Ming (Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Zeng, Hui (Department of Bone & Joint Surgery, Peking University Shenzhen Hospital)
  • 투고 : 2020.12.31
  • 심사 : 2021.01.15
  • 발행 : 2022.03.25

초록

Many studies have shown that Mg-Nd-Zn-Zr (abbreviated as JDBM) alloy has good biocompatibility and biodegradability as well as promotion of cell adhesion, proliferation and differentiation, and Wnt/β-catenin signaling pathway may play a unique role in joint tissue by controlling the function of chondrocytes, osteoblasts and synoviocytes. However, it is not clear whether the JDBM alloy induces osteochondral repair through Wnt/β-catenin signaling pathway. This study aims to verify that JDBM alloy can repair osteochondral defects in rats, which is realized by Wnt/β-catenin signaling pathway. In this study, the osteochondral defect model of the right femoral condyle non-weight-bearing area in rats was established and randomly divided into three groups: Control group, JDBM alloy implantation group and JDBM alloy implantation combined with signaling pathway inhibitor drug ICRT3 injection. It was found that after JDBM alloy implantation, the bone volume fraction (BVF) became larger, the bone trabeculae were increased, the relative expression of osteogenesis gene Runx2, Bmp2, Opn, Ocn and chondrogenesis gene Collagen II, Aggrecan were increased, and the tissue repair was obvious by HE and Masson staining, which could be inhibited by ICRT3.

키워드

과제정보

This study was supported by grants from National Natural Science Foundation of China (No. 82172432, 82102568 and 82001319), National & Local Joint Engineering Research Center of Orthopaedic Biomaterials (No. XMHT20190204007), Shenzhen High-level Hospital Construction Fund, Shenzhen Key Medical Discipline Construction Fund (No. SZXK023), Shenzhen "San-Ming" Project of Medicine (No. SZSM201612092), Guangdong Basic and Applied Basic Research Foundation (No. 2021A1515012586 and 2019A1515011290), Bethune Charitable Foundation and CSPC Osteoporosis Research Foundation Project (No. G-X-2020-1107-21), Shenzhen Research and Development Projects (No. JCYJ20210318153832004), Sustainable development project of Science and Technology in Shenzhen (No. KCXFZ20201221173411031), and Scientific Research Foundation of PEKING UNIVERSITY SHENZHEN HOSPITAL (No. KYQD2021099).

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